HCCS Activators
The chemical activation of HCCS, a key enzyme in the biosynthesis of holocytochrome c, is tightly regulated by the availability of substrates and cofactors within the mitochondrial environment. Specific compounds that increase the availability of iron, such as iron-containing porphyrins and various iron salts, directly contribute to the catalytic efficiency of HCCS. For instance, the presence of iron in its ferrous state, maintained by reducing agents, is vital for heme synthesis, which is subsequently covalently attached to apocytochrome c by HCCS. Additionally, the modulation of heme synthesis through the depletion of heme levels can trigger compensatory upregulation of HCCS to restore heme synthesis. The cellular redox state, influenced by reducing agents, is also crucial as it ensures the heme iron is in the correct oxidation state, thereby facilitating HCCS activity. Moreover, the induction of mitochondrial biogenesis increases the demand for cytochrome c, indirectly enhancing HCCS function within the mitochondria to meet the biosynthetic needs.
On the other hand, the stabilization of hypoxia-inducible factors under mimic hypoxic conditions elevates the synthesis of heme proteins, indirectly increasing HCCS activity. This upregulation is further supported by compounds that can chelate iron, creating a state of perceived deficiency which then encourages the upregulation of mechanisms to synthesize more heme, consequently stimulating the activity of HCCS. Additionally, certain molecules that release nitric oxide can impact the activity of heme-containing enzymes, and by influencing the stability and availability of heme can indirectly affect the activity of HCCS. Lastly, the availability of NADH as a coenzyme in mitochondrial redox reactions signifies an increased metabolic activity, thereby potentially enhancing the synthesis of holocytochrome c and the functional activity of HCCS in response to the elevated energetic demands of the cell.
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Hemin chloride | 16009-13-5 | sc-202646 sc-202646A sc-202646B | 5 g 10 g 25 g | $102.00 $160.00 $326.00 | 9 | |
Hemin is an iron-containing porphyrin. It binds to apocytochrome c, facilitating the final enzymatic step in which HCCS catalyzes the covalent attachment of heme to cytochrome c, thereby increasing its activity. | ||||||
Copper(II) sulfate | 7758-98-7 | sc-211133 sc-211133A sc-211133B | 100 g 500 g 1 kg | $46.00 $122.00 $189.00 | 3 | |
Copper(II) sulfate provides copper ions that can act as cofactors in electron transfer reactions. This can enhance the functional activity of HCCS as it involves electron transfer during the attachment of heme to cytochrome c. | ||||||
Zinc | 7440-66-6 | sc-213177 | 100 g | $48.00 | ||
Zinc sulfate supplies zinc ions which can stabilize the structure of heme proteins and potentially facilitate the HCCS-mediated synthesis of holocytochrome c by enhancing the proper folding and function of the protein. | ||||||
L-Ascorbic acid, free acid | 50-81-7 | sc-202686 | 100 g | $46.00 | 5 | |
Ascorbic acid acts as a reducing agent and can maintain iron in its ferrous state. This is essential for the heme synthesis pathway, indirectly supporting HCCS activity by ensuring the availability of the correct heme iron valence state for binding to apocytochrome c. | ||||||
Succinylacetone | 51568-18-4 | sc-212963 sc-212963B | 10 mg 100 mg | $336.00 $418.00 | ||
Succinylacetone is a heme synthesis inhibitor known to deplete heme levels. The reduction in heme may upregulate compensatory mechanisms, including HCCS, to restore heme synthesis. | ||||||
L-Leucine | 61-90-5 | sc-364173 sc-364173A | 25 g 100 g | $21.00 $62.00 | ||
L-Leucine has been shown to upregulate mitochondrial biogenesis, which could indirectly increase the demand for cytochrome c and thus enhance the functional activity of HCCS in heme attachment. | ||||||
Iron(II) sulfate solution | 10028-21-4 | sc-224024 | 1 each | $46.00 | ||
Ferrous sulfate provides a source of ferrous iron, a necessary component of the heme group. This can indirectly promote HCCS activity by ensuring adequate iron supply for heme synthesis. | ||||||
Cobalt(II) chloride | 7646-79-9 | sc-252623 sc-252623A | 5 g 100 g | $64.00 $176.00 | 7 | |
Cobalt(II) chloride can mimic hypoxic conditions by stabilizing hypoxia-inducible factors (HIFs). HIF stabilization can lead to increased synthesis of heme proteins, indirectly enhancing HCCS activity. | ||||||
Deferoxamine | 70-51-9 | sc-507390 | 5 mg | $255.00 | ||
Deferoxamine is an iron chelator that can create a deficiency of free iron, potentially upregulating heme synthesis pathways and indirectly stimulating HCCS activity to compensate for the reduced iron availability. | ||||||
NADH disodium salt | 606-68-8 | sc-205762 sc-205762A | 500 mg 1 g | $91.00 $127.00 | 3 | |
An essential coenzyme in redox reactions and mitochondrial function. Increased mitochondrial activity could indirectly increase the need for holocytochrome c synthesis, thus potentially enhancing HCCS activity. | ||||||